Lauren A. Plante

Misoprostol vaginal insert and time to vaginal delivery: a randomized controlled trial.

OBJECTIVE: To compare the efficacy and safety of a 200-microgram misoprostol vaginal insert with a 10-mg dinoprostone vaginal insert for reducing the time to vaginal delivery. METHODS: In a phase III, double-blind, multicenter study, women being induced with a modified Bishop score of 4 or less were randomly assigned to receive either a 200-microgram misoprostol vaginal insert or a 10-mg dinoprostone vaginal insert. Coprimary end points were time to vaginal delivery and rate of cesarean delivery. Secondary end points included time to any delivery mode, time to onset of active labor, and oxytocin use. RESULTS: A total of 1,358 women were randomized to receive the 200-microgram misoprostol vaginal insert (n=678) or dinoprostone vaginal insert (n=680). Women receiving the misoprostol vaginal insert had a significantly shorter median time to vaginal delivery compared with patients receiving the dinoprostone vaginal insert (21.5 hours compared with 32.8 hours, P<.001). Cesarean delivery occurred in 26.0% and 27.1% of women receiving the misoprostol vaginal insert and dinoprostone vaginal insert, respectively. A significant reduction in time to any delivery (18.3 hours compared with 27.3 hours), time to onset of active labor (12.1 hours compared with 18.6 hours), and proportion of women requiring predelivery oxytocin (48.1% compared with 74.1%) was observed with the misoprostol vaginal insert compared with dinoprostone vaginal insert (P<.001 for each). Uterine tachysystole requiring intervention occurred in 13.3% and 4.0% of participants receiving the misoprostol vaginal insert and dinoprostone vaginal insert, respectively (P<.001). CONCLUSION: Use of a 200-microgram misoprostol vaginal inset significantly reduced times to vaginal delivery and active labor with reduced need for oxytocin compared with the dinoprostone vaginal insert. Cesarean delivery rates were similar with both treatments. Tachysystole was more common in women receiving the 200-microgram misoprostol vaginal insert. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, www.clinicaltrials.gov, NCT01127581. LEVEL OF EVIDENCE: I

Circulating Cell-Free DNA to Determine the Fetal RHD Status in All Three Trimesters of Pregnancy.

OBJECTIVE: To estimate the accuracy of a new assay to determine the fetal RHD status using circulating cell-free DNA. METHODS: This was a prospective, observational study. Maternal blood samples were collected in each trimester of pregnancy in 520 nonalloimmunized RhD-negative patients. Plasma samples were analyzed for circulating cell-free DNA using the SensiGENE RHD test, which used primers for exons 4 and 7 as previously described and incorporated a new primer design for exon 5 of the RHD gene. Neonatal serology for RhD typing using cord blood at birth was undertaken and results were stored in a separate clinical database. After unblinding the data, results of the DNA analysis were compared with the neonatal serology. RESULTS: Inconclusive results secondary to the presence of the RHD pseudogene or an RHD variant were noted in 5.6%, 5.7%, and 6.1% of the first-, second-, and third-trimester samples, respectively. The incidence of false-positive rates for RhD (an RhD-negative fetus with an RHD-positive result) was 1.54% (95% confidence interval [CI] 0.42–5.44%), 1.53% (CI 0.42–5.40%), and 0.82% (CI 0.04–4.50%), respectively. There was only one false-negative diagnosis (an RhD-positive fetus with an RHD-negative result), which occurred in the first trimester (0.32%; 95% CI 0.08–1.78%). Genotyping for mismatches across repeated samples revealed that this error was related to mislabeling of samples from two patients collected on the same day at one of the collection sites. Overall test results were in agreement across all three trimesters (P>.99). CONCLUSION: Circulating cell-free DNA can accurately predict the fetal RhD status in all three trimesters of pregnancy.

Placenta membranacea with placenta accreta: radiologic diagnosis and clinical implications.

Placenta membranacea, also called placenta diffusa, is a rare developmental abnormality of the human placenta in which fetal membranes are covered diffusely by chorionic villi of varying thickness. Although its etiology remains elusive, several reports have linked this entity to abnormal placental adherence, as well as life-threatening antepartum hemorrhage and fetal death. We searched MEDLINE using PubMed for all English-language articles published until 2013 with search terms ‘placenta membranacea’, ‘placenta diffusa’, ‘placenta accreta’, ‘hemorrhage’, and ‘cesarean hysterectomy.’ Our search returned 18 publications pertaining to this subject. In all publications, the diagnosis of placenta membrancea was achieved by post-delivery pathologic examination of the placenta. On the basis of this search, our report represents the first case of the antenatal diagnosis of placenta membranacea using magnetic resonance imaging (MRI). A 21-year-old African-American woman presented for routine ultrasonography (US) at a gestational age of 22weeks and 3days. The patient underwent a full-term cesarean delivery 1 year ago for fetal intolerance to labor. Although US imaging revealed fetal biometry consistent with gestational age, the placenta was visualized diffusely throughout the uterus, appearing thinner than usual (Figure 1). Placenta membranacea was suspected, and the patient was scheduled for monthly US evaluation of placental and fetal growth. On subsequent US imaging, the placenta appeared thinner that is, <2 standard deviations below the mean thickness, and was visualized throughout the anterior and posterior walls of the uterus, with portions suspicious for abnormal adherence. Given the suspicion of abnormal placental adherence, MRI of the abdomen and pelvis was performed at gestational age of 32weeks and 3 days. Using gradient-echo T1-weighted, T2-weighted, and T2 fat-saturated sequences, the placenta was now seen covering greater than 75% of the inner myometrial surface. Loss of normal myometrial-placental interface in multiple areas was also noted. This was particularly evident along the posterior wall of the uterus (Figure 2), particularly at the level of the aortic bifurcation. The descending colon appeared to immediately abut the uterine wall, suspicious for infiltration of placental tissue through the left lateral uterus into the wall of the colon. Multiple placental venous lakes within the posterior left placenta measuring up to 3.7 × 5.5 × 3.8 cm were also visualized. Interestingly, the anterior lower uterine segment, which was the site of the previous uterine incision, was the only portion of the uterus free of placenta. These findings confirmed the presence of placenta membranacea with several areas suspicious for placenta percreta particularly along the posterior uterine wall. In anticipation of complicated surgery and the possibility of life-threatening intraoperative hemorrhage, we formulated a meticulous plan of having ready availability of blood products, specialized intraoperative surgical, anesthesia and nursing staff, as well as immediate postoperative intensive care monitoring. Given the findings of placenta membranacea with several areas suspicious for placenta percreta, we planned to proceed with a cesarean hysterectomy under general anesthesia between 34 and 35weeks of gestational age. At a gestational age of 34weeks and 2 days, the patient was taken to the operating room, where US-guided placental mapping was performed prior to abdominal entry. A 10 cm midline vertical skin incision was created, and a live male infant weighing 2495 g and APGAR scores of 4/8 was delivered through a low-transverse hysterotomy. Despite no intraoperative evidence of placenta percreta along the posterior or anterior uterine wall, we still suspected at least a placenta accreta and deemed the large placental mass not amenable to delivery through the hysterotomy. We, therefore, proceeded with the cesarean hysterectomy. The placenta was left in situ, and an uneventful subtotal hysterectomy was

RGS2 squelches vascular Gi/o and Gq signaling to modulate myogenic tone and promote uterine blood flow.

Uterine artery blood flow (UABF) is critical to maintaining uterine perfusion in nonpregnant states and for uteroplacental delivery of nutrients and oxygen to the fetus during pregnancy. Impaired UABF is implicated in infertility and several pregnancy complications including fetal growth restriction, small for gestational age, and preeclampsia. The etiology of abnormal UABF is not known. Here, we determined whether deficiency or loss of RGS2, a GTPase‐activating protein for Gq/11 and Gi/o class G proteins, affects UABF in nonpregnant mice. We used Doppler ultrasonography to assess UABF in wild type (WT), Rgs2 heterozygous (Rgs2+/−), and homozygous knockout (Rgs2−/−) mice. Video microscopy was used for ex vivo examination of uterine artery myogenic tone and fura‐2 imaging for in vitro assessment of internal stores Ca2+ release. We found that baseline UABF velocity was markedly decreased while impedance measured as resistive index (WT = 0.58 ± 0.04 vs. Rgs2−/− = 0.71 ± 0.03, P < 0.01) and pulsatile index (WT = 0.90 ± 0.06 vs. Rgs2−/− = 1.25 ± 0.11, P < 0.01) was increased in Rgs2−/− mice. Uterine artery tone was augmented in Rgs2+/− and Rgs2−/− mice, which was normalized to WT levels following Gi/o and Gq inactivation. Conversely, blockade of ryanodine receptors increased WT myogenic tone to RGS2 mutant levels. The data together indicate that RGS2 deficiency decreases UABF by increasing myogenic tone at least partly through prolonged G protein activation. Mutations that decrease vascular RGS2 expression may be a predisposition to decreased uterine blood flow. Targeting G protein signaling therefore might improve uterine and uteroplacental underperfusion disorders.

Management of Sepsis and Septic Shock for the Obstetrician–Gynecologist

The incidence of sepsis is increasing in the United States, both in the general adult population and among pregnant and postpartum women. Neither infection nor bacteremia are synonymous with sepsis: it is a dysregulated host response to a pathogen in which organ dysfunction is key. New clinical criteria have been released. Cornerstones of management are early suspicion and recognition, effective fluid resuscitation, and appropriate antimicrobial therapy.

Maternal Critical Care: A Multidisciplinary Approach

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Antenatal testing in uncomplicated pregnancies: should testing be initiated after 40 or 41 weeks?

Abstract Objective: This study aims to compare outcomes of antenatal testing in women who received testing between 40 weeks and 40+6 weeks versus those who received testing at ≥41 weeks. Materials and methods: This retrospective study included women without maternal comorbidities, who were referred for outpatient antenatal testing for gestational age ≥40 weeks. We compared women who received antenatal testing between 40 and 40+6 weeks (Group 1), to those who were only tested at ≥41 weeks (Group 2). Results: A total of 827 Group 1 and 244 Group 2 pregnancies were evaluated. One-hundred and eighty-nine (18%) were sent to labor and delivery (L&D) for further evaluation. There were no significant differences between groups in terms of being sent or admitted to labor and delivery, the reason for which women were sent, induction of labor, mode of delivery, neonatal length of stay, or admission to intensive care. Conclusion: Pregnancies tested at 40 weeks were identified as abnormal and sent to L&D at the same rate as those tested at 41 weeks. Therefore, it may be reasonable to initiate fetal surveillance at the estimated date of delivery.

Vaginorectal streptococcus porcinus in pregnancy: An emerging pathogen?

Objective Streptococcus porcinus has previously been isolated from the genitourinary tract of reproductive-aged women. However, very little is known about the pathogenicity of this microorganism in pregnancy. The study aimed to report pregnancies complicated by vaginorectal S. porcinus and associated adverse outcomes. Materials and Methods We present 2 patients with 3 pregnancies complicated by vaginorectal S. porcinus and preterm cervical change. Results The first patient lost a twin pregnancy to previable preterm rupture of membranes. During her subsequent pregnancy, again positive for S. porcinus, cervical shortening prompted antibiotic treatment and cerclage. The second patient delivered preterm despite cerclage placed for sonographic indications. Conclusions Our cases suggest that S. porcinus may contribute to the pathogenesis of preterm rupture of membranes and cervical insufficiency.

Obstetric Disorders in the ICU

Abstract Pregnant and postpartum patients represent a challenge to critical care physicians, as two patients in one have to be cared for and because specific obstetric disorders, not universally covered in formal critical care training, need to be managed. Pregnancy also alters physiologic norms, so that the critical care physician may either fail to recognize a value as abnormal in pregnancy or mistakenly identify as abnormal a value within the normal range for a pregnant woman. In this article, we will review the most frequent obstetric causes of admission of pregnant/postpartum patients to the intensive care unit (hypertensive disease of pregnancy, obstetric hemorrhage, and obstetric sepsis) along with their diagnostic criteria, clinical presentation, and recommended treatment. We will also cover some specific, although less frequent, obstetric disorders, such as acute fatty liver of pregnancy, peripartum cardiomyopathy, and amniotic fluid embolism. Our primary aim is to improve quality of care for these types of patients.

Maternal Critical Care: Contents

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